Steroid Use and Its Effects on the Musculoskeletal System

Two Distinct Categories of Steroids

The word "steroids" encompasses two pharmacologically distinct classes with very different clinical profiles: corticosteroids (glucocorticoids and mineralocorticoids), used therapeutically to reduce inflammation and suppress immune activity, and anabolic-androgenic steroids (AAS), derivatives of testosterone used to enhance muscle mass and performance. The mechanisms, risks, and musculoskeletal effects of each are substantially different and are addressed separately here.

Corticosteroids: Benefits and Musculoskeletal Costs

Corticosteroids — including prednisolone, methylprednisolone, hydrocortisone, and dexamethasone — are among the most widely prescribed medications globally, used for conditions ranging from asthma and inflammatory bowel disease to rheumatoid arthritis and polymyalgia rheumatica. Their therapeutic value in controlling inflammatory and autoimmune disease is substantial and often life-changing. Their musculoskeletal costs, however, accumulate with duration and dose.

Corticosteroid-induced osteoporosis is the most clinically significant consequence. Glucocorticoids suppress osteoblast activity and increase osteoclast-mediated bone resorption, producing a net reduction in bone mineral density. The rate of bone loss is most rapid in the first three to six months of therapy. Vertebral fractures — often occurring with minimal or no trauma — are the most common complication, with a fracture risk approximately doubled even at low doses (5–7.5mg prednisolone/day) sustained over six months.

Steroid myopathy is a well-recognised pattern of proximal muscle weakness affecting the shoulder girdle, hip girdle, and anterior thigh — essentially the same distribution as polymyalgia rheumatica, which can create diagnostic confusion in patients on corticosteroids for PMR. It develops through multiple mechanisms: inhibition of muscle protein synthesis, enhanced protein catabolism, impaired mitochondrial function, and type II muscle fibre atrophy. It is dose-dependent and typically improves on dose reduction, though recovery can be slow.

Tendon and soft tissue effects include impaired fibroblast function, reduced collagen synthesis, and altered tendon mechanical properties. These effects are most pronounced following local injection and explain why repeated corticosteroid injections into a specific tendon carry meaningful rupture risk.

Anabolic-Androgenic Steroids: The Performance Price

AAS misuse accelerates muscle growth at a rate that outpaces connective tissue adaptation. The fundamental problem is that testosterone drives rapid increases in muscle cross-sectional area and force production capacity, but tendon and ligament adaptation to increased load is a slower, mechanically-mediated process. The resulting force-capacity mismatch places tendons under supra-physiological loading.

The clinical consequence is a well-documented elevated incidence of spontaneous tendon rupture — particularly of the distal biceps, Achilles, quadriceps, and patellar tendons. These ruptures often occur during activities that would be considered sub-maximal for the individual's apparent muscle development. Imaging frequently shows pre-existing tendon degeneration (tendinosis) at the rupture site, suggesting the risk accumulates progressively rather than arising from a single acute event.

Post-cycle, the withdrawal of supraphysiological testosterone produces a period of relative hypogonadism — the hypothalamic-pituitary-gonadal axis, suppressed by exogenous androgen, does not recover immediately. This produces fatigue, depression, reduced libido, and — most relevantly in the rehabilitation context — significantly impaired capacity for muscle protein synthesis and connective tissue repair, precisely at the time when injuries are most likely.

Clinical Considerations for Practitioners

Patients on long-term corticosteroids require modified treatment approaches. Mobilisation and exercise prescription should account for elevated fracture risk — heavy axial loading of the spine and high-impact activities require careful consideration. Vitamin D and calcium supplementation, and in many cases bisphosphonate therapy, are clinically recommended for patients on corticosteroids for more than three months.

In manual therapy, direct pressure over osteoporotic vertebrae in patients on long-term corticosteroids warrants care; vertebral fragility fractures can be precipitated by forces that would be entirely benign in a healthy skeleton. Similarly, the diagnosis of steroid myopathy should be considered when a patient on corticosteroids reports progressive proximal weakness disproportionate to their disease activity — a phenomenon that will not improve with massage and requires dose review.